Listeria monocytogenes

[1][2][3] In the European Union, listeriosis continues an upward trend that began in 2008, causing 2,161 confirmed cases and 210 reported deaths in 2014, 16% more than in 2013.

[3] Once Listeria monocytogenes enters the host cytoplasm, multiple changes in bacterial metabolism and gene expression help to complete its metamorphosis from soil dweller to intracellular pathogen.

Due to its frequent pathogenicity, causing meningitis in newborns (acquired transvaginally), pregnant women are often advised not to eat soft cheeses such as Brie, Camembert, feta, and queso blanco fresco, which may be contaminated with and permit growth of L.

L. monocytogenes serotype 4b strains are responsible for 33 to 35% of sporadic human cases worldwide and for all major foodborne outbreaks in Europe and North America since the 1980s.

[16] Murray referred to the organism as Bacterium monocytogenes before Harvey Pirie changed the genus name to Listeria in 1940.

[18] Listeriosis in adults was later associated with patients living with compromised immune systems, such as individuals taking immunosuppressant drugs and corticosteroids for malignancies or organ transplants, and those with HIV infection.

An outbreak of listeriosis in Halifax, Nova Scotia, involving 41 cases and 18 deaths, mostly in pregnant women and neonates, was epidemiologically linked to the consumption of coleslaw containing cabbage that had been contaminated with L. monocytogenes-contaminated sheep manure.

[20] Since then, a number of cases of foodborne listeriosis have been reported, and L. monocytogenes is now widely recognized as an important hazard in the food industry.

The manifestations of listeriosis include sepsis,[22] meningitis (or meningoencephalitis),[22] encephalitis,[23] corneal ulcer,[24] pneumonia,[25] myocarditis,[26] and intrauterine or cervical infections in pregnant women, which may result in spontaneous abortion (second to third trimester) or stillbirth.

An early study suggested that L. monocytogenes is unique among Gram-positive bacteria in that it might possess lipopolysaccharide,[27] which serves as an endotoxin.

These lipoteichoic acids resemble the lipopolysaccharides of Gram-negative bacteria in both structure and function, being the only amphipathic polymers at the cell surface.

From cases contracted through raw or supposedly pasteurized milk, one may safely assume that, in susceptible persons, fewer than 1,000 total organisms may cause disease.

Its presence intracellularly in phagocytic cells also permits access to the brain and probably transplacental migration to the fetus in pregnant women.

It seems that Listeria originally evolved to invade membranes of the intestines, as an intracellular infection, and developed a chemical mechanism to do so.

When this bacterium is present within a host organism, quorum sensing and other signals cause the up-regulation of several virulence genes.

[36] Little is known about how this bacterium switches between acting as a saprophyte and a pathogen; however, several noncoding RNAs are thought to be required to induce this change.

[citation needed] L. monocytogenes has three distinct lineages, with differing evolutionary histories and pathogenic potentials.

[37] The Anton test is used in the identification of L. monocytogenes; instillation of a culture into the conjunctival sac of a rabbit or guinea pig causes severe keratoconjunctivitis within 24 hours.

Identification is enhanced if the primary cultures are done on agar containing sheep blood, because the characteristic small zone of hemolysis can be observed around and under colonies.

[41] The motility at room temperature and hemolysin production are primary findings that help differentiate Listeria from Corynebacterium.

Total time to identification takes five to seven days, but the announcement of specific non-radiolabelled DNA probes should soon allow a simpler and faster confirmation of suspect isolates.

[citation needed] When listeric meningitis occurs, the overall mortality may reach 70%, from sepsis 50%, and from perinatal/neonatal infections greater than 80%.

One example of the successful use of L. monocytogenes in in vitro transfer technologies is in the delivery of gene therapies for cystic fibrosis cases.

[48][49] A live attenuated Listeria monocytogenes cancer vaccine, ADXS11-001, is under development as a possible treatment for cervical carcinoma.

Listeria monocytogenes is quite hardy and resists the deleterious effects of freezing, drying, and heat remarkably well for a bacterium that does not form spores.

[53] The primary site of infection is the intestinal epithelium, where the bacteria invade nonphagocytic cells via the "zipper" mechanism.

[56] The ability of L. monocytogenes to successfully infect depends on its resistance to the high concentrations of bile encountered throughout the gastrointestinal tract.

Stages in the intracellular lifecycle of L. monocytogenes : (Center) Cartoon depicting entry, escape from a vacuole, actin nucleation, actin-based motility, and cell-to-cell spread. (Outside) Representative electron micrographs from which the cartoon was derived. LLO, PLCs, and ActA are all described in the text. The cartoon and micrographs were adapted from Tilney and Portnoy (1989).
Colonies of typical L. monocytogenes as they appear when grown on Listeria -selective agar